Mapping residual transmission for malaria elimination

  1. Robert C Reiner  Is a corresponding author
  2. Arnaud Le Manach
  3. Simon Kunene
  4. Nyasatu Ntshalintshali
  5. Michelle S Hsiang
  6. T Alex Perkins
  7. Bryan Greenhouse
  8. Andrew J Tatem
  9. Justin M Cohen
  10. David L Smith
  1. National Institutes of Health, United States
  2. Clinton Health Access Initiative, United States
  3. National Malaria Control Program, Swaziland
  4. University of Texas Southwestern Medical Center, United States
  5. University of California, San Francisco, United States

Abstract

Eliminating malaria from a defined region involves draining the endemic parasite reservoir and minimizing local malaria transmission around imported malaria infections1. In the last phases of malaria elimination, as universal interventions reap diminishing marginal returns, national resources must become increasingly devoted to identifying where residual transmission is occurring. The needs for accurate measures of progress and practical advice about how to allocate scarce resources require new analytical methods to quantify fine-grained heterogeneity in malaria risk. Using routine national surveillance data from Swaziland (a sub-Saharan country on the verge of elimination), we estimated individual reproductive numbers. Fine-grained maps of reproductive numbers and local malaria importation rates were combined to show `malariogenic potential,' a first for malaria elimination. As countries approach elimination, these individual-based measures of transmission risk provide meaningful metrics for planning programmatic responses and prioritizing areas where interventions will contribute most to malaria elimination.

Article and author information

Author details

  1. Robert C Reiner

    Fogarty International Center, National Institutes of Health, Bethesda, United States
    For correspondence
    rcreiner@indiana.edu
    Competing interests
    The authors declare that no competing interests exist.
  2. Arnaud Le Manach

    Clinton Health Access Initiative, Boston, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Simon Kunene

    National Malaria Control Program, Manzini, Swaziland
    Competing interests
    The authors declare that no competing interests exist.
  4. Nyasatu Ntshalintshali

    Clinton Health Access Initiative, Boston, United States
    Competing interests
    The authors declare that no competing interests exist.
  5. Michelle S Hsiang

    Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, United States
    Competing interests
    The authors declare that no competing interests exist.
  6. T Alex Perkins

    Fogarty International Center, National Institutes of Health, Bethesda, United States
    Competing interests
    The authors declare that no competing interests exist.
  7. Bryan Greenhouse

    Department of Medicine, University of California, San Francisco, San Francisco, United States
    Competing interests
    The authors declare that no competing interests exist.
  8. Andrew J Tatem

    Fogarty International Center, National Institutes of Health, Bethesda, United States
    Competing interests
    The authors declare that no competing interests exist.
  9. Justin M Cohen

    Clinton Health Access Initiative, Boston, United States
    Competing interests
    The authors declare that no competing interests exist.
  10. David L Smith

    Fogarty International Center, National Institutes of Health, Bethesda, United States
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Mark Jit, London School of Hygiene & Tropical Medicine, and Public Health England, United Kingdom

Version history

  1. Received: June 18, 2015
  2. Accepted: November 26, 2015
  3. Accepted Manuscript published: December 29, 2015 (version 1)
  4. Version of Record published: January 27, 2016 (version 2)

Copyright

© 2015, Reiner et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 2,913
    views
  • 705
    downloads
  • 53
    citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Robert C Reiner
  2. Arnaud Le Manach
  3. Simon Kunene
  4. Nyasatu Ntshalintshali
  5. Michelle S Hsiang
  6. T Alex Perkins
  7. Bryan Greenhouse
  8. Andrew J Tatem
  9. Justin M Cohen
  10. David L Smith
(2015)
Mapping residual transmission for malaria elimination
eLife 4:e09520.
https://doi.org/10.7554/eLife.09520

Share this article

https://doi.org/10.7554/eLife.09520

Further reading

    1. Medicine
    2. Neuroscience
    Yunlu Xue, Yimin Zhou, Constance L Cepko
    Research Advance

    Retinitis pigmentosa (RP) is an inherited retinal disease in which there is a loss of cone-mediated daylight vision. As there are >100 disease genes, our goal is to preserve cone vision in a disease gene-agnostic manner. Previously we showed that overexpressing TXNIP, an α-arrestin protein, prolonged cone vision in RP mouse models, using an AAV to express it only in cones. Here, we expressed different alleles of Txnip in the retinal pigmented epithelium (RPE), a support layer for cones. Our goal was to learn more of TXNIP’s structure-function relationships for cone survival, as well as determine the optimal cell type expression pattern for cone survival. The C-terminal half of TXNIP was found to be sufficient to remove GLUT1 from the cell surface, and improved RP cone survival, when expressed in the RPE, but not in cones. Knock-down of HSP90AB1, a TXNIP-interactor which regulates metabolism, improved the survival of cones alone and was additive for cone survival when combined with TXNIP. From these and other results, it is likely that TXNIP interacts with several proteins in the RPE to indirectly support cone survival, with some of these interactions different from those that lead to cone survival when expressed only in cones.

    1. Medicine
    Peigen Chen, Haicheng Chen ... Xing Yang
    Research Article

    Caesarean section scar diverticulum (CSD) is a significant cause of infertility among women who have previously had a Caesarean section, primarily due to persistent inflammatory exudation associated with this condition. Even though abnormal bacterial composition is identified as a critical factor leading to this chronic inflammation, clinical data suggest that a long-term cure is often unattainable with antibiotic treatment alone. In our study, we employed metagenomic analysis and mass spectrometry techniques to investigate the fungal composition in CSD and its interaction with bacteria. We discovered that local fungal abnormalities in CSD can disrupt the stability of the bacterial population and the entire microbial community by altering bacterial abundance via specific metabolites. For instance, Lachnellula suecica reduces the abundance of several Lactobacillus spp., such as Lactobacillus jensenii, by diminishing the production of metabolites like Goyaglycoside A and Janthitrem E. Concurrently, Clavispora lusitaniae and Ophiocordyceps australis can synergistically impact the abundance of Lactobacillus spp. by modulating metabolite abundance. Our findings underscore that abnormal fungal composition and activity are key drivers of local bacterial dysbiosis in CSD.